首页> 美国卫生研究院文献>Genetics >Detection of Rsp and Modifier Variation in the Meiotic Drive System SEGREGATION DISTORTER (SD) of DROSOPHILA MELANOGASTER
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Detection of Rsp and Modifier Variation in the Meiotic Drive System SEGREGATION DISTORTER (SD) of DROSOPHILA MELANOGASTER

机译:DROSOPHILA MELANOGASTER减数分裂驱动系统SEGREGATION DISTORTER(SD)中Rsp和修饰子变化的检测

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摘要

Identification of allelic variability at the two major loci ( Sd and Rsp) that interact to cause sperm dysfunction in Segregation distorter (SD) males of D. melanogaster has been hampered by the difficulty in separating the elements recombinationally. In addition, small differences in the strength of Sd alleles or sensitivities of Rsp alleles to Sd are difficult to measure against background genetic or environmental variation. Viability effects of the markers used to score progeny classes may also introduce a bias. Removal of Sd and E(SD) from their second chromosome location to create a Dp(2;Y)Sd E(SD) chromosome eliminates these problems, since any combination of Rsp alleles can be easily tested without resorting to recombinational techniques. Further, since these pairs of Rsp alleles are compared in their response to Dp Sd E(SD) in the same individual males, background variation and viability effects can be easily removed to allow finescale resolution of Rsp differences. Tests of all possible pairwise combination of six laboratory chromosomes in this way revealed at least three and possibly four different Rsp allelic classes. In addition, the hierarchical nature of the tests further allowed for determination of the presence of linked suppressors or enhancers of Sd activity. A sample of 11 second chromosomes selected from a group recently isolated from a natural population was also unambiguously ordered as to Rsp allelic status using this approach. The resultant pattern was similar to that obtained for the laboratory chromosomes, except for the not unexpected observation that the natural population apparently harbored more drive suppressors. The pattern of results obtained from these pairwise combinations of Rsp alleles supports the notion that there are no dominance interactions within the group, but that each responds more or less independently to Sd in giving sperm dysfunction.
机译:在两个主要基因座(Sd和Rsp)处相互作用的等位基因变异的鉴定已被困难地阻碍了重组分离元素的障碍,这两个主要基因座相互作用导致了D. melanogaster的分离畸变(SD)男性的精子功能障碍。此外,很难根据背景遗传或环境变化来衡量Sd等位基因强度或Rsp等位基因对Sd敏感性的微小差异。用于对子代类别进行评分的标记的生存力效应也可能会产生偏差。从第二个染色体位置去除Sd和E(SD)以创建Dp(2; Y)Sd E(SD)染色体消除了这些问题,因为 Rsp 等位基因的任何组合都可以轻松测试而无需诉诸重组技术。此外,由于在同一男性个体中比较了这对 Rsp 等位基因对 Dp Sd E SD )的反应,因此背景变异和可以轻松消除生存力影响,以实现 Rsp 差异的精细分辨率。以这种方式对六个实验室染色体的所有可能的成对组合进行的测试显示出至少三个,可能是四个不同的 Rsp 等位基因类别。另外,测试的等级性质进一步确定了 Sd 活性的连锁抑制子或增强子的存在。还使用这种方法明确地确定了从最近从自然种群中分离出来的11个第二条染色体的样本,以确定它们的 Rsp 等位基因状态。所得到的模式与实验室染色体获得的模式相似,只是不出意外的观察,即自然种群显然具有更多的驱动抑制因子。从这些 Rsp 等位基因的成对组合获得的结果模式支持以下观点:该组内没有优势相互作用,但每种相互作用或多或少地独立于 Sd 给精子功能障碍。

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